PMID- 9779824
OWN - NLM
STAT- MEDLINE
DCOM- 19981222
LR  - 20191024
IS  - 0730-2312 (Print)
IS  - 0730-2312 (Linking)
VI  - 71
IP  - 2
DP  - 1998 Nov 1
TI  - Hepatocyte growth factor/scatter factor and hepatocytes are potent downregulators 
      of tyrosinase expression in B16 melanoma cells.
PG  - 264-76
AB  - Reiterated selection in vivo of B16 murine melanoma cells for enhanced liver 
      metastatic ability yielded a cel line (B16-LS9) dramatically overexpressing a 
      constitutively active hepatocyte growth factor/scatter factor (HGF/SF) receptor, 
      the product of the c-met proto-oncogene. Most likely because of their 
      overexpressing c-met, B16-LS9 cells appear to be more responsive than parental 
      B16-F1 cells to HGF stimulation, in terms of motility, invasion, and growth. They 
      are also more pigmented, and express higher levels of tyrosinase as compared to 
      parental B1 6-F1 cells. Therefore, we set out to explore whether HGF/SF and the 
      liver might influence the differentiation state of B1 6 cells. We found that 
      HGF/SF and MSH, two factors which reportedly have a strong influence on the 
      phenotype and the malignant behavior of melanoma cells, may act at different 
      levels, and with opposite results, on the regulation of gene expression. In fact, 
      while MSH induces, at the transcriptional level, an increase in the production of 
      both c-met and tyrosinase, HGF/SF, in contrast, promotes a decrease in the 
      expression of both c-met and tyrosinase, however at a posttranscriptional level. 
      These two opposite effects can counter-balance each other, when the cells are 
      treated with both factors at the same time, apparently through a mechanism 
      involving MAP kinase activation. The effects were, however, additive when 
      morphological changes were considered. Most intriguingly, we also describe a very 
      strong downregulatory activity, limited to tyrosinase expression, by hepatocytes 
      in coculture with B16 cells. This activity, also at the posttranscriptional 
      level, is much stronger than that exerted by HGF/SF, and appears to be due to a 
      labile soluble factor produced by the hepatocytes.
FAU - Rusciano, D
AU  - Rusciano D
AD  - Friedrich Miescher Institute, Basel, Switzerland. rusciano@fmi.ch
FAU - Lorenzoni, P
AU  - Lorenzoni P
FAU - Lin, S
AU  - Lin S
FAU - Burger, M M
AU  - Burger MM
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - 9002-79-3 (Melanocyte-Stimulating Hormones)
RN  - EC 1.14.18.1 (Monophenol Monooxygenase)
SB  - IM
MH  - Animals
MH  - Cell Differentiation
MH  - Down-Regulation/*physiology
MH  - Gene Expression Regulation, Enzymologic/physiology
MH  - Hepatocyte Growth Factor/*physiology
MH  - Melanocyte-Stimulating Hormones/physiology
MH  - Melanoma, Experimental/*enzymology/pathology
MH  - Monophenol Monooxygenase/genetics/*physiology
MH  - Tumor Cells, Cultured
EDAT- 1998/10/21 02:04
MHDA- 2000/06/20 09:00
CRDT- 1998/10/21 02:04
PHST- 1998/10/21 02:04 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1998/10/21 02:04 [entrez]
AID - 10.1002/(SICI)1097-4644(19981101)71:2<264::AID-JCB11>3.0.CO;2-L [pii]
AID - 10.1002/(sici)1097-4644(19981101)71:2<264::aid-jcb11>3.0.co;2-l [doi]
PST - ppublish
SO  - J Cell Biochem. 1998 Nov 1;71(2):264-76. doi: 
      10.1002/(sici)1097-4644(19981101)71:2<264::aid-jcb11>3.0.co;2-l.